My long-term goal is to establish a successful independent research career and make significant contributions to the field of lung biology. My graduate and postdoctoral training involved the use of a variety of molecular and cellular approaches to the study of gene expression in mammalian tissues. My entry into the area of lung embryology is relatively recent and represents a new research direction. I am the recipient of a NIH RO1 grant funded by the NHLBI, attesting to my research potential as an independent investigator. Environment and institutional commitment: I hold a faculty position at the USC Center for Craniofacial Molecular Biology. This highly interactive, state- of-the-art research center has provided full support for my independent research efforts and is committed to my continued research development. Career development plan: I expect to devote essentially full-time effort to laboratory and research- related activities. I plan to develop my career by acquiring new research skills and increasing my knowledge of lung development and lung disease through both intramural and extramural course work, attending seminars, workshops, and meetings, and through formation of new collaborations and new interactions with both basic and clinical scientists. Research plan: I am interested in understanding the molecular mechanism by which Smad-mediated TGF- beta signaling regulates early lung development. My research plan addresses the following hypothesis: Specific Smad gene expression regulates TGF-beta signaling, and thus instructs early mouse embryonic lung branching morphogenesis. The Specific Aims are: (1). To define the developmental and temporo-spatial expression of Smad genes during embryonic lung development (i) in vivo and (ii) in lung explant culture; (2). To determine the molecular mechanism of TGF-beta pathway-restricted Smad2 and Smad3 in regulating embryonic pulmonary morphodifferentiation in culture using both (i) "loss-of-function" and (ii) "gain-of- function" strategies; (3). To define the biological function of the feedback inhibitory Smad6 and Smad7 proteins during embryonic lung branching morphogenesis in culture. The current study of the molecular embryology will provide new rationales for novel therapeutic strategies to modulate TGF-beta signaling during lung injury and disease.